New studies have provided surprising results regarding the effects of vitamin D in situations other than calcium and phosphate homeostasis. As they report in this issue, Zhang et al. studied mice deficient in the vitamin D nuclear receptor and induced diabetes by injection of streptozotocin. They found that diabetic mice lacking the vitamin D receptor had more severe albuminuria and glomerulosclerosis than their wild-type controls. Further, these animals expressed more transforming growth factor- (TGF-) and developed more sclerosis by deposition of a number of extracellular matrix proteins such as fibronectin. Recent studies published in Kidney International showed that vitamin D receptor is a transcriptional regulator of renin; in the present paper, the authors found that renin, angiotensinogen, and connective tissue growth factor increased in the kidneys of receptor knockout mice. These in vivo studies were supplemented by in vitro studies showing that 1,25-dihydroxyvitmain D3 inhibited high glucose, induced fibronectin production in cultured mesangial cells, and increased nephrin expression in cultured podocytes, as well as suppressing the activation of the renin–angiotensin system and TGF- in mesangial and juxtaglomerular cells. These findings demonstrate that vitamin D and its receptor play a salutary role in the pathogenesis of fibrosis in diabetic nephropathy.

Top of pageBiocompatible peritoneal dialysis solutions

Kidney International is often accused of failing to publish negative studies; we now have an interesting one. Peritoneal dialysis fluids are 'unnatural' in that they have compositions quite different from that of body fluids in general. Their high glucose levels and other components are thought to lead to inflammation and eventual fibrosis of the peritoneal membranes. The development of 'biocompatible' solutions was thus hailed as a definitive advance in this field; a number of studies have shown that these solutions are better in that they reduce inflammation and protect the peritoneal membranes from the dreaded peritoneal failure due to fibrosis. Yet no randomized controlled studies had been published comparing the use of biocompatible with standard solutions. A new study by Fan et al. now compares the two types of solutions. After a 1-year follow-up in a group of patients with similar clinical states, the authors found no significant difference in urea, creatinine clearance, or secondary end points between the two groups. This finding is disappointing, but it shows that logic can be wrong in scientific studies. However, the search for better dialysis solutions must continue, since the cause of peritoneal fibrosis and inflammation is clearly the solution itself. See page 200.

Top of pageFructose and kidney stones

Countless papers on fructose and kidney disease have been done, many of them recently published. In this issue, Taylor and Curhan describe the relationship between fructose intake and incident kidney stones in the Nurses' Health Study I (93 730 older women), the Nurses' Health Study II, and the Health Professionals Follow-up Study (45,984 men). They estimated fructose intake every 4 years on the basis of food frequency questionnaires. Cox proportional hazard regressions were adjusted for age, body mass index, thiazide use, caloric intake, and other dietary factors. During a combined 48 years of follow-up, almost 5,000 stone episodes were identified. Patients with the highest fructose intake had a higher incidence of kidney stones than those with the lowest fructose intake. This effect seemed to be specific for fructose, as the intake of other carbohydrates was not associated with risk of kidney stones. These surprising results raise the question of the potential mechanism by which this sugar leads to increased risk of kidney stones. Investigation of the mechanism is an urgent issue given that the intake of fructose is increasing, at least in industrialized countries.